Post-concussion, infection, migraine change, and hallucinogen use drove 42% of VS cases; secondary cases showed significantly greater improvement at follow-up (p <.001).
🔬 Clinical Considerations
- 42% of VS cases had identifiable triggers: post-concussion (15), dramatic migraine/aura change (14), post-infection (13), and HPPD (10) led secondary causes; secondary cases improved at 3x the rate of spontaneous cases (30.3% vs. 8.3%)
- Treatable underlying causes include IIH, ocular pathology, neoplasm, and MS: two patients had demyelinating disease; four had IIH; one resolved after temporal lobe tumor resection and radiation
- No medication provided complete remission; partial response rates: lamotrigine 17%, topiramate 6%, benzodiazepines highest responder rate, acetazolamide 21% in IIH-associated cases
- Anxiety was significantly more prevalent in primary VS (58% vs. 36%, p=.002), while palinopsia and floaters also tracked with spontaneous onset
🎯 Practice Applications
- Obtain brain MRI with gadolinium, ophthalmologic exam, and funduscopy for papilledema in all new-onset VS presentations
- Screen for IIH by history (transient visual obscurations, whooshing tinnitus) before attributing VS to primary etiology
- Counsel patients with identifiable triggers that partial improvement is possible, particularly when the underlying cause is addressable
- Consider EEG when VS onset coincides with suspected seizure activity or features of neurodegeneration
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